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Semax

Also identified as ACTH (4-10) analogue, Met-Glu-His-Phe-Pro-Gly-Pro

Synthetic ACTH(4-10) analogue

Sequence: Met-Glu-His-Phe-Pro-Gly-Pro

Molecular weight
813.9
Molecular formula
C37H51N9O10S
CAS
80714-61-0
Published studies reviewed
3

FOR RESEARCH USE ONLY. NOT FOR HUMAN OR VETERINARY USE. NOT FOR HUMAN CONSUMPTION.

Compounds described on this site are supplied solely for laboratory research. They are not offered for human or veterinary use or for clinical use, and they are not intended to diagnose, mitigate, cure or prevent any disease.

Semax is the synthetic heptapeptide Met-Glu-His-Phe-Pro-Gly-Pro, an analogue of the adrenocorticotropin fragment ACTH(4-10). Three publications are reviewed: a 2006 rat study of BDNF and trkB markers in the hippocampus, a binding study on rat brain membranes, and a study of its copper chemistry. The mechanism its authors propose rests on rat measurements, and no human study is represented.

At a glance

Also identified as
ACTH (4-10) analogue, Met-Glu-His-Phe-Pro-Gly-Pro
Class
Synthetic ACTH(4-10) analogue
Target or mechanism
BDNF/trkB system (rat hippocampus)
Evidence types represented
in vitro, animal
Published studies reviewed
3
Last reviewed
2026-09-24

Overview

Semax is a synthetic heptapeptide, Met-Glu-His-Phe-Pro-Gly-Pro, described in the literature as an analogue of the adrenocorticotropin fragment ACTH(4-10).

One of the three publications recorded on this page, a 2006 study, measured what a single application of Semax did to the BDNF/trkB system in the rat hippocampus. Four things were measured and four things are reported: BDNF protein, phosphorylation of the trkB receptor, and the messenger RNA levels of each. The same study also counted conditioned avoidance reactions in the treated animals.

Every one of those measurements was made in a rat. The authors propose that the BDNF/trkB system is how Semax affects brain function; that proposal is theirs, it is about rats, and this page records it as a proposal rather than restating it as a finding about people.

Nothing here is a statement about the research material PepGenex supplies.

Mechanism under investigation

Semax
Neuropeptide analogue
  • BDNF/trkB system (rat hippocampus)

The 2006 study recorded here measured BDNF protein, trkB receptor phosphorylation and the messenger RNA for both, in the rat hippocampus, following a single application. The authors propose modulation of that system as the mechanism; the measurements supporting it are entirely in rats.

Scope of the published work

Areas investigated
  • BDNF expression
  • trkB receptor phosphorylation
  • Conditioned avoidance behaviour
Models used
  • Rat hippocampus

Of the three publications recorded here, one is a rat study measuring molecular markers in one brain region after a single application, and two are laboratory studies: one of binding to rat brain membranes, one of copper chemistry. No human study is represented. Nothing on this page is a statement about the research material PepGenex supplies.

Limitations

Evidence represented on this page: in vitro and animal. No human research is represented. The page reviews 3 published studies, and each figure is reported for the study that published it; results are not pooled across studies.

Common questions

What is Semax?

Semax is a synthetic heptapeptide, Met-Glu-His-Phe-Pro-Gly-Pro, described in the literature as an analogue of the adrenocorticotropin fragment ACTH(4-10).

How does Semax work, according to the published research?

The 2006 study recorded here measured BDNF protein, trkB receptor phosphorylation and the messenger RNA for both, in the rat hippocampus, following a single application. The authors propose modulation of that system as the mechanism; the measurements supporting it are entirely in rats.

  • Equilibrium studies of Semax with copper(II) showed three complex species. Two minor species, [CuL] and [CuLH-1]-, coexisted with [CuLH-2]2- between pH 3.6 and 5; from pH 5 the [CuLH-2]2- species became predominant, with the donor atoms around copper arranged in a 4N planar coordination mode. (Tabbì et al., 2015, PMID 25310602)
  • Homogeneously tritium-labelled [G-3H]Semax bound plasma membranes of the rat forebrain basal nuclei in a time-dependent, specific and reversible manner. Specific binding depended on calcium ions and was characterised by Kd = 2.41 ± 1.02 × 10⁻⁹ M and Bmax = 33.5 ± 7.9 × 10⁻¹⁵ mol/mg of protein. (Dolotov et al., 2004, PMID 15344653)

What has published research on Semax found, and what are its limits?

This page records 3 publications, reporting laboratory (in vitro) work in 2, animal work in 1. Each is listed with its identifier under References.

No human study is represented on this page.

Related publications, cited by identifier:

Evidence represented on this page: in vitro and animal.

No human research is represented.

The page reviews 3 published studies, and each figure is reported for the study that published it; results are not pooled across studies.

Of the three publications recorded here, one is a rat study measuring molecular markers in one brain region after a single application, and two are laboratory studies: one of binding to rat brain membranes, one of copper chemistry. No human study is represented. Nothing on this page is a statement about the research material PepGenex supplies.

  • Panikratova et al. 2020, "Functional Connectomic Approach to Studying Selank and Semax Effects": a resting-state functional MRI study in healthy participants that included a Semax group. Its findings are recorded on the Selank page. (PMID 32342318)
  • Kost et al. 2001, "Semax and selank inhibit the enkephalin-degrading enzymes from human serum": a laboratory study in human serum. Its findings are recorded on the Selank page. (PMID 11443939)

Is Semax approved by the U.S. FDA?

This page cites no FDA approval record for Semax; PepGenex Science states a U.S. regulatory status only where a sourced record exists.

PepGenex research materials are not FDA approved and are not for human or veterinary use.

What risks have published studies of Semax reported?

No human study is recorded on this page, so it reports no adverse events in people. Laboratory and animal findings are not a measure of risk in people.

Published research

Grouped by the kind of study. Select one to narrow what is shown below.

Laboratory (in vitro)(2)

Laboratory (in vitro)

Semax, an ACTH4-10 peptide analog with high affinity for copper(II) ion and protective ability against metal induced cell toxicity

Tabbì G, Magrì A, Giuffrida A, et al., Journal of Inorganic Biochemistry, 2015;142:39-46

published

  • Semax was described as a heptapeptide encompassing the 4-7 sequence of the N-terminal domain of adrenocorticotropic hormone (ACTH) joined to a C-terminal Pro-Gly-Pro tripeptide.
  • Equilibrium studies of Semax with copper(II) showed three complex species. Two minor species, [CuL] and [CuLH-1]-, coexisted with [CuLH-2]2- between pH 3.6 and 5; from pH 5 the [CuLH-2]2- species became predominant, with the donor atoms around copper arranged in a 4N planar coordination mode.
View publication →
Laboratory (in vitro)

The binding of Semax, ACTH 4-10 heptapeptide, to plasma membranes of the rat forebrain basal nuclei and its biodegradation

Dolotov OV, Zolotarev IuA, Dorokhova EM, et al., Bioorganicheskaia Khimiia, 2004;30(3):241-246

published

  • Homogeneously tritium-labelled [G-3H]Semax bound plasma membranes of the rat forebrain basal nuclei in a time-dependent, specific and reversible manner. Specific binding depended on calcium ions and was characterised by Kd = 2.41 ± 1.02 × 10⁻⁹ M and Bmax = 33.5 ± 7.9 × 10⁻¹⁵ mol/mg of protein.
  • In the presence of rat brain plasma membranes, Semax had a half-life longer than 1 hour. Dipeptidylaminopeptidases were considered the main enzymes responsible for its degradation, successively cleaving it to the pentapeptide HFPGP and the tripeptide PGP.
View publication →

Preclinical (animal)(1)

Preclinical (animal)

Semax, an analog of ACTH(4-10) with cognitive effects, regulates BDNF and trkB expression in the rat hippocampus

Dolotov OV, Karpenko EA, Inozemtseva LS, et al., Brain Research, 2006;1117(1):54-60

published

A single dose of Semax in rats, with BDNF and trkB measured in the hippocampus, alongside a count of conditioned avoidance reactions.

  • A maximal 1.4-fold increase in BDNF protein levels was reported in the rat hippocampus following a single application.
  • A 1.6-fold increase in trkB tyrosine phosphorylation was reported in the rat hippocampus, accompanying the change in BDNF protein.
  • A 3-fold increase in exon III BDNF messenger RNA was reported in the rat hippocampus.
  • A 2-fold increase in trkB messenger RNA was reported in the rat hippocampus.
  • The animals given Semax showed a distinct increase in the number of conditioned avoidance reactions. This is a behavioural count in rats, reported alongside the molecular measurements.
What this study establishes

Four separate measurements moved in the same direction after a single application: BDNF protein, phosphorylation of its receptor, and the messenger RNA for each. Four coherent measurements are more informative than one, because they describe a system responding rather than a single number moving.

Limitations

The system responding is a rat's. The publication measures molecules in one brain region and counts a learned behaviour in the same animals; it does not measure anything in a person, and the step from a fold-change in rat hippocampal mRNA to a statement about human thinking is not a step this study licenses anyone to take.

View publication →

Compared with related compounds

Classification, structure, recorded targets, evidence types and FDA status only, each read from the two compounds' own pages. These comparisons do not compare study results.

Semax and Selank

Synthetic heptapeptide analogues of natural peptide fragments: ACTH(4-10) and tuftsin.

SemaxSelank
ClassificationSynthetic ACTH(4-10) analogueTuftsin analogue
StructureSequence Met-Glu-His-Phe-Pro-Gly-Pro; formula C37H51N9O10SSequence Thr-Lys-Pro-Arg-Pro-Gly-Pro; formula C33H57N11O9
Targets recordedBDNF/trkB system (rat hippocampus)Enkephalin-degrading enzymes of human plasma and serum; [3H]GABA binding sites on brain cell plasma membranes
Evidence types representedin vitro, animalin vitro, animal, human
Status with the U.S. FDANot shown (no Drugs@FDA application record verified for this page)Not shown (no Drugs@FDA application record verified for this page)

References

Published studies reviewed (3)

  1. Semax, an analog of ACTH(4-10) with cognitive effects, regulates BDNF and trkB expression in the rat hippocampus — Dolotov OV, Karpenko EA, Inozemtseva LS, et al., Brain Research, 2006;1117(1):54-60
    DOI 10.1016/j.brainres.2006.07.108 · PMID 16996037
  2. The binding of Semax, ACTH 4-10 heptapeptide, to plasma membranes of the rat forebrain basal nuclei and its biodegradation — Dolotov OV, Zolotarev IuA, Dorokhova EM, et al., Bioorganicheskaia Khimiia, 2004;30(3):241-246
    DOI 10.1023/b:rubi.0000030127.46845.f0 · PMID 15344653
  3. Semax, an ACTH4-10 peptide analog with high affinity for copper(II) ion and protective ability against metal induced cell toxicity — Tabbì G, Magrì A, Giuffrida A, et al., Journal of Inorganic Biochemistry, 2015;142:39-46
    DOI 10.1016/j.jinorgbio.2014.09.008 · PMID 25310602

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